ライフサイエンスコーパス: aquaporin 4

1 NMO-IgG reacts with the water channel aquaporin 4.

2 nd validate a subset on endogenous astrocyte Aquaporin 4.

3 ight junction protein zonula occludens 1 and aquaporin 4.

4 against the astrocytic water channel protein aquaporin-4.

5 toantibodies against astrocyte water channel aquaporin-4.

6 dies against the glial water channel protein aquaporin-4.

7 cellular volume by means of ion channels and aquaporin-4.

8 olecular target of NMO-IgG was identified as aquaporin-4.

9 0.3) in mice lacking the glial water channel aquaporin-4.

10 -null mouse which lacks sarcolemmal nNOS and aquaporin-4.

11 ting its effect via the perivascular pool of aquaporin-4.

12 as LGI1, N-methyl-D-aspartate receptor, and aquaporin-4.

13 tiedema effects via the perivascular pool of aquaporin-4, 2) hypertonic saline attenuates blood-brain

14 chloride cotransporter-1, 2.8-fold increase; aquaporin 4, 8.9-fold increase (3.6-fold increase in chr

15 Markers of mature astrocytes, including aquaporin 4 (a water channel in astrocyte endfeet) and i

16 crease in GFAP and inflammatory proteins and aquaporin-4, a glymphatic system protein that assists in

17 ce Ags (myelin oligodendrocyte glycoprotein, aquaporin 4, acetylcholine receptor, and muscle-specific

18 sociated with astrocytic proteins, including aquaporin 4, actin, and glutamine synthetase and serine

19 eally injected NMO-IgG binds mouse placental aquaporin-4, activates coinjected human complement, and

20 synthetase, glutamate transporter 1 (GLT1), aquaporin-4, aldehyde dehydrogenase 1 family member L1,

21 and 3) deletion of the perivascular pool of aquaporin-4 alleviates tissue damage after stroke, in mi

22 unity control cohort, autoantibodies against aquaporin 4 and high-titer Abs against myelin oligodendr

23 known to modulate edema formation, including aquaporin-4 and AMP-activated protein kinase and its dow

24 R/MYOC overexpression, including homologs of aquaporin-4 and cytochrome-P450, previously associated w

25 In conclusion, we identify aquaporin-4 and GPRC5B as old and new players in genetic

26 also trigger an autoimmune reaction against aquaporin-4 and inflammation of the CNS.

27 tic and expressed increased levels of water (aquaporin-4) and ion (Kir4.1) channels.

28 on depending on the presence of perivascular aquaporin-4, and 3) deletion of the perivascular pool of

29 luding eight sites among aquaporin-2 (AQP2), aquaporin-4, and urea transporter isoforms A1 and A3.

30 ic neuritis and myelitis and the presence of aquaporin 4 antibodies (AQP4-abs).

31 Testing for aquaporin 4 antibodies was undertaken in all suspected c

32 Aquaporin 4 antibodies were tested using 2 sensitive ass

33 Patients with neuromyelitis optica who have aquaporin-4 antibodies are being identified and receivin

34 raightforward when the highly specific serum aquaporin-4 antibodies are detected with cell-based assa

35 rtunistic retinal infection in patients with aquaporin-4 antibodies who are receiving immunosuppressa

36 nistic infections can occur in patients with aquaporin-4 antibodies who are receiving relatively low

37 We describe 2 patients with aquaporin-4 antibodies who were receiving conventional d

38 Aquaporin 4 antibody (AQP4-Ab)-negative patients with lo

39 sability Status Scale score), change in anti-aquaporin 4 antibody, and safety of rituximab treatment.

40 Aquaporin 4 antibody-negative neuromyelitis optica (NMO)

41 come, and prognostic features in relation to Aquaporin-4 antibody (AQP4-Ab) status, and compared to a

42 and are used in treatment monitoring; but in aquaporin-4 antibody neuromyelitis optica spectrum disor

43 etrospective observational case series of 14 aquaporin-4 antibody positive NMO and NMO spectrum disor

44 The patient population included a ratio of aquaporin-4 antibody seropositive and seronegative patie

45 iple sclerosis but has not been evaluated in aquaporin-4 antibody seropositive neuromyelitis optica s

46 al, we enrolled adults aged 18-74 years with aquaporin-4 antibody seropositive or seronegative NMOSD

47 acerbation of MOGAD and NMOSD (regardless of aquaporin-4 antibody status), and were significantly hig

48 rlaps between MOGAD, multiple sclerosis, and aquaporin-4 antibody-associated neuromyelitis optica spe

49 py is mainly based on standard protocols for aquaporin-4 antibody-associated NMOSD and multiple scler

50 itor ravulizumab in adult patients with anti-aquaporin-4 antibody-positive (AQP4+) neuromyelitis opti

51 O according to Wingerchuk's 2006 criteria or aquaporin-4 antibody-positive NMO spectrum disorder (NMO

52 We report 12 aquaporin-4 antibody-positive patients (12% of seroposit

53 tcomes and prognostic characteristics of 106 aquaporin-4 antibody-seropositive patients from the UK a

54 METHOD: (1) Retrospective cohort of 76 aquaporin 4-antibody (AQP4-Ab)-positive patients from Ox

55 (1) Retrospective cohort of 76 aquaporin 4-antibody (AQP4-Ab)-positive patients from Ox

56 dren with ADEM, seizures, encephalitis, anti-aquaporin-4-antibody (AQP4-Ab)-seronegative neuromyeliti

57 etrospective study we included patients with aquaporin-4-antibody seropositive NMOSD (n = 28), MOGAD

58 Aquaporin 4 (AQ4) is not expressed in the choroid plexus

59 ina revealed that an increased expression of aquaporin-4 (AQP-4) in the flight mice compared to contr

60 oantibodies targeting the astroglial protein aquaporin 4 (AQP4) and leads to vision loss, motor defic

61 against the astrocyte water channel protein aquaporin 4 (AQP4) and the evidence that AQP4-IgG is inv

62 cooperation between the glial water channel aquaporin 4 (AQP4) and the transient receptor potential

63 Aquaporin 4 (AQP4) appeared distributed all over the cel

64 The glymphatic system, that is aquaporin 4 (AQP4) facilitated exchange of CSF with inte

65 neuritis (ON), the presence of antibodies to aquaporin 4 (AQP4) has diagnostic and prognostic value.

66 tive for MOG-IgA and double-seronegative for aquaporin 4 (AQP4) IgG and MOG-IgG.

67 d protein) and supramolecular aggregation of aquaporin 4 (AQP4) in mouse, rat, and human tissues.

68 staining showed aberrant co-localization of aquaporin 4 (AQP4) in retracted GFAP+ astrocytes with di

69 Aquaporin 4 (AQP4) is highly expressed at perivascular g

70 Aquaporin 4 (AQP4) is highly expressed in the glial cell

71 tion after binding of an IgG autoantibody to aquaporin 4 (AQP4) is thought to be a major determinant

72 Water channel aquaporin 4 (AQP4) plays a key role in the regulation of

73 ostasis.SIGNIFICANCE STATEMENT Water channel aquaporin 4 (AQP4) plays a key role in the regulation of

74 Moreover, mRNA expression of water channel, aquaporin 4 (AQP4) was increased after Dp71 deletion.

75 receptor potential isoform 4 (TRPV4) and the aquaporin 4 (AQP4) water channel in retinal Muller cells

76 tic transport due to genetic deletion of the aquaporin 4 (AQP4) water channel showed exacerbation of

77 ection of IgG autoantibodies that target the aquaporin 4 (AQP4) water channel, which, in the CNS, is

78 Modulation of the aquaporin 4 (AQP4) water-regulatory channel or productio

79 brain to edema formation by up-regulation of aquaporin 4 (AQP4), a water channel in the brain that ha

80 Aquaporins, particularly aquaporin 4 (Aqp4), are membrane proteins with important

81 tion of an astrocytic water channel protein, Aquaporin 4 (AQP4), is known to predominantly contribute

82 f the perivascular pool of the water channel aquaporin 4 (AQP4), suggesting that an efficient clearan

83 by pathogenetic serum IgG autoantibodies to aquaporin 4 (AQP4), the most abundant water-channel prot

84 Aquaporin 4 (AQP4)-specific autoantibodies in neuromyeli

85 2) and the astrocyte-specific water channel, aquaporin 4 (AQP4).

86 e expression of the astrocytic water channel aquaporin-4 (AQP4) and changes in glymphatic pathway fun

87 In adult retina, aquaporin-4 (AQP4) and inwardly rectifying K(+) (Kir4.1)

88 onally, loss of astrocytic laminin decreases aquaporin-4 (AQP4) and tight junction protein expression

89 However, since the discovery of NMO-IgG or aquaporin-4 (AQP4) antibody (AQP4-antibody), an NMO-spec

90 toantibodies against astrocyte water channel aquaporin-4 (AQP4) are highly specific for the neuroinfl

91 toantibodies against astrocyte water channel aquaporin-4 (AQP4) are thought to be pathogenic in neuro

92 M23" isoform of the glial cell water channel aquaporin-4 (AQP4) assembles into orthogonal arrays of p

93 ral nervous system caused by binding of anti-aquaporin-4 (AQP4) autoantibodies (NMO-IgG) to AQP4 on a

94 role of interleukin (IL)-6 and complement in aquaporin-4 (AQP4) autoimmunity remains unclear.

95 ogy compatible with targeting of sarcolemmal aquaporin-4 (AQP4) by complement-activating IgG implies

96 Aquaporin-4 (AQP4) can assemble into supramolecular aggr

97 bulin [Ig]G) against astrocyte water channel aquaporin-4 (AQP4) cause complement- and cell-mediated a

98 ogenic autoantibodies (NMO-IgG) to astrocyte aquaporin-4 (AQP4) causes complement-dependent cytotoxic

99 Aquaporin-4 (AQP4) deficiency in mice reduces neuroinfla

100 Aquaporin-4 (AQP4) deletion slowed K(+) reuptake about t

101 with reduced reactive gliosis and polarized aquaporin-4 (AQP4) distribution.

102 oimmune disease caused by antibodies against aquaporin-4 (AQP4) expressed on astrocytes.

103 was no significant alteration in ipsilateral Aquaporin-4 (AQP4) expression following MCAO or progeste

104 Perivascular localization of aquaporin-4 (AQP4) facilitates the clearance of intersti

105 The astroglial water channel aquaporin-4 (AQP4) facilitates water movement into and o

106 ress the mercurial-insensitive water channel aquaporin-4 (AQP4) for purification and reconstitution.

107 The glial water channel protein aquaporin-4 (AQP4) forms heterotetramers in the plasma m

108 The water channel aquaporin-4 (AQP4) forms supramolecular clusters whose s

109 The aquaporin-4 (AQP4) gene encodes proteins of approximatel

110 Two major isoforms of aquaporin-4 (AQP4) have been described in human tissue.

111 rin-1 (AQP1) in microvascular endothelia and aquaporin-4 (AQP4) in airway epithelia.

112 d peptides in multiple sclerosis (MS) and to aquaporin-4 (AQP4) in neuromyelitis optica spectrum diso

113 The organization of aquaporin-4 (AQP4) into large plasma membrane assemblies

114 Aquaporin-4 (AQP4) is a mercurial-insensitive, water-sel

115 Aquaporin-4 (AQP4) is a primary influx route for water d

116 Aquaporin-4 (AQP4) is a water channel protein expressed

117 Aquaporin-4 (AQP4) is a water transport protein expresse

118 Aquaporin-4 (AQP4) is a water-selective transport protei

119 Aquaporin-4 (AQP4) is enriched at the sarcolemma of skel

120 The astrocyte water channel aquaporin-4 (AQP4) is expressed as heterotetramers of M1

121 The water channel protein aquaporin-4 (AQP4) is expressed in astrocytes and mediat

122 Aquaporin-4 (AQP4) is found on the basolateral plasma me

123 Aquaporin-4 (AQP4) is the major water channel expressed

124 Aquaporin-4 (AQP4) is the major water channel in the bra

125 Aquaporin-4 (AQP4) is the major water channel in the CNS

126 Aquaporin-4 (AQP4) is the primary water channel in the m

127 ort system is supported by the water channel aquaporin-4 (AQP4) localized to vascular endfeet of astr

128 eposition, as well as an astrocytopathy with aquaporin-4 (AQP4) loss.

129 Using an aquaporin-4 (AQP4) M1-isoform-specific enzyme-linked imm

130 the brain involves movement of water through aquaporin-4 (AQP4) membrane channels.

131 sts that the Muller/glial cell water channel aquaporin-4 (AQP4) modulates K(+) channel function of th

132 toantibodies (NMO-immunoglobulin G [IgG]) to aquaporin-4 (AQP4) on astrocytes, which initiates comple

133 cytic processes (labeled with antibodies for aquaporin-4 (AQP4) or glial fibrillary acidic protein we

134 r recruitment of the water-permeable channel aquaporin-4 (AQP4) to astrocytic endfeet is dependent on

135 ular localization of the brain water channel aquaporin-4 (AQP4) was investigated during the neurologi

136 biogenesis, hydrophilic peptide loops of the aquaporin-4 (AQP4) water channel are delivered to cytoso

137 toimmune CNS disorder mediated by pathogenic aquaporin-4 (AQP4) water channel autoantibodies (AQP4-Ig

138 The Aquaporin-4 (AQP4) water channel contributes to brain wa

139 The astrocytic aquaporin-4 (AQP4) water channel is the target of pathog

140 toantibodies (NMO-IgGs) directed against the aquaporin-4 (AQP4) water channel located on astrocyte fo

141 colleagues show that the two isoforms of the aquaporin-4 (AQP4) water channel may determine the fate

142 Aquaporin-4 (AQP4) water channel-specific IgG distinguis

143 Here, we examined the role of aquaporin-4 (AQP4) water channels after experimental con

144 Aquaporin-4 (AQP4) water channels are expressed strongly

145 re electron microscopy (FFEM) indicates that aquaporin-4 (AQP4) water channels can assemble in cell p

146 earance mechanism additionally suggests that aquaporin-4 (AQP4) water channels facilitate convective

147 Tetramers of aquaporin-4 (AQP4) water channels form supramolecular as

148 s optica-immunoglobulin G (NMO-IgG) binds to aquaporin-4 (AQP4) water channels in the central nervous

149 The plasma membrane assembly of aquaporin-4 (AQP4) water channels into orthogonal arrays

150 Aquaporin-4 (AQP4) water channels on astrocytic end-feet

151 This autoantibody targets astrocytic aquaporin-4 (AQP4) water channels.

152 Here we show that mice deficient in aquaporin-4 (AQP4), a glial membrane water channel, have

153 s, disrupts the perivascular localization of aquaporin-4 (AQP4), a water channel essential for glymph

154 Aquaporin-4 (AQP4), a water channel expressed in astrocy

155 ous studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following b

156 MO patients carry IgG autoantibodies against aquaporin-4 (AQP4), an astrocytic water channel.

157 fusion in the ECS was faster in mice lacking aquaporin-4 (AQP4), an astroglial water channel that fac

158 Determination of antibodies to NMDAR, aquaporin-4 (AQP4), and myelin oligodendrocyte glycoprot

159 toantibodies against astrocyte water channel aquaporin-4 (AQP4), called AQP4-IgG.

160 e-specific major water channel in the brain, aquaporin-4 (AQP4), in brain plasticity and learning.

161 -IgGs) against supra-molecular assemblies of aquaporin-4 (AQP4), known as orthogonal array of particl

162 Subsequently, aquaporin-4 (AQP4), the most abundant water channel in t

163 rum autoantibody biomarker, NMO-IgG, targets aquaporin-4 (AQP4), the most abundant water channel prot

164 Aquaporin-4 (AQP4), the primary water channel in glial c

165 Aquaporin-4 (AQP4), the principal water channel in astro

166 he extent of a brain-specific water channel, aquaporin-4 (AQP4), using confocal and electron microsco

167 e discovery of serum antibodies (Ab) against aquaporin-4 (AQP4), which unequivocally differentiate NM

168 ed by ELISA in patients with NMOSD (n=39, 28 aquaporin-4 (AQP4)-Ab-seropositive, 3 double-Ab-seronega

169 isation of GABA(A) receptors (GABA(A)Rs) and aquaporin-4 (AQP4)-containing protein complexes in neuro

170 ord MRIs for ring-enhancing lesions from 284 aquaporin-4 (AQP4)-IgG seropositive patients at Mayo Cli

171 le serum on live cell-based assays (CBA) for aquaporin-4 (AQP4)-M23-IgG and myelin-oligodendrocyte gl

172 By developing an aquaporin-4 (Aqp4)-mRuby3 knock-in reporter mouse that a

173 ptic neuritis, multiple sclerosis (MS), anti-aquaporin-4 (AQP4)-negative neuromyelitis optica (NMO),

174 Aquaporin-4 (AQP4)-specific T cells are expanded in neur

175 Aquaporin-4 (AQP4)-specific Th17 cells are thought to ha

176 ibodies (NMO-IgG) to astrocyte water channel aquaporin-4 (AQP4).

177 c autoantibodies (NMO-IgG) against astrocyte aquaporin-4 (AQP4).

178 against the astrocyte water channel protein aquaporin-4 (AQP4).

179 lin G [IgG]) against astrocyte water channel aquaporin-4 (AQP4).

180 re often seropositive for antibodies against aquaporin-4 (AQP4).

181 trogliosis, and mislocalization of astrocyte aquaporin-4 (AQP4).

182 er fluxes augmented by vasopressin-regulated aquaporin-4 (AQP4).

183 pectrum disorder have autoantibodies against aquaporin-4 (AQP4-Abs), but recently, myelin-oligodendro

184 ure to an antibody to the astrocytic protein aquaporin-4 (AQP4-IgG) in mice.

185 conserved C-terminally elongated variant of Aquaporin 4 (AQP4X), which is exclusively perivascular.

186 is activated and, IP(3) R, TRPA1, TRPV4, and Aquaporin-4 are all involved in shaping the dynamics of

187 The discovery of aquaporin-4 as the putative target of NMO-IgG, and recen

188 Aquaporin-4 assembles in astrocyte plasma membranes as s

189 GFAP-aquaporin 4 association decreased during initial sucklin

190 reduced and then increased the expression of aquaporin 4, astrocytic water channels coupled to K(+) c

191 d maintained expression of the water channel aquaporin-4 at astrocytic perivascular endfeet of the BB

192 t the Delta PDZ form, reestablished nNOS and aquaporin-4 at the sarcolemma of these mice.

193 disorder (NMOSD) patients harbor serum anti-aquaporin-4 autoantibodies targeting astrocytes in the C

194 e investigated whether immunoglobulin G from aquaporin-4-autoantibody-positive neuromyelitis optica p

195 ing in the setting of neoplasia suggest that aquaporin-4 autoimmunity may in some cases have a parane

196 athogenic IgG that competes with NMO-IgG for aquaporin-4 binding, significantly reduced NMO-IgG and h

197 AQP4-IgG binding to aquaporin-4 causes complement-dependent cytotoxicity (CD

198 cyclinD1, fibulin 2, tenascin C, TIMP1, and aquaporin-4, correlations were significantly nonlinear,

199 rted previously that astroglia cultured from aquaporin-4-deficient (AQP4-/-) mice migrate more slowly

200 Data suggest that autoantibodies to aquaporin 4 derived from peripheral B cells cause the ac

201 mportant in determining clinical outcomes in aquaporin-4 disease.

202 n molecules are excluded from the GJ plaque (Aquaporin 4, EAAT2b), while others are quite penetrant (

203 hich recognize the immunodominant epitope of aquaporin-4, exhibit Th17 polarization and cross-react w

204 This is associated with increased aquaporin 4 expression in the intestinal mucosa and subm

205 At a molecular level, aquaporin-4 expression decreased and the expression and

206 Placental aquaporin-4 expression is high during mid-gestation and

207 man complement, there was a striking loss of aquaporin-4 expression, glial cell oedema, myelin breakd

208 components, extensive demyelination, loss of aquaporin-4 expression, loss of reactive astrocytes and

209 Aquaporin-4 facilitates the influx of Abeta in brain-eye

210 earance of amyloid beta, and the fraction of Aquaporin 4 found perivascularly is decreased in Alzheim

211 This is associated with up-regulation of aquaporin 4 gene expression and protein.

212 may indicate stem cell-capabilities whereas aquaporin 4 has been reported to promote the osmorecepto

213 dy responses to the astrocytic water channel aquaporin 4 have been described.

214 OSD whose test results were seropositive for aquaporin-4 IgG and who had a hepatic metastasis from a

215 icrocystic changes in terms of age, sex, and aquaporin 4-IgG antibody status.

216 Thirty-nine patients with aquaporin 4-IgG seropositive NMOSD (age: 50.1+/-14.1 yea

217 ange, 13-81 years); 84% were women; 80% were aquaporin 4-IgG seropositive; and the median Expanded Di

218 n both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG coexisted (71%).

219 ence (on December 31, 2011) of NMO/NMOSD and aquaporin-4-IgG seroincidence and seroprevalence (sera c

220 idemiological studies are limited by lack of aquaporin-4-IgG seroprevalence assessment, absence of po

221 Aquaporin-4-IgG was measured by M1-isoform-fluorescent-a

222 in antibody-associated disease (MOGAD) (92), aquaporin-4-IgG-positive neuromyelitis optica spectrum d

223 ociated disease (MOGAD) and differences from aquaporin-4-IgG-positive-neuromyelitis-optica-spectrum-d

224 ng diseases (IDD) with a specific biomarker, aquaporin-4-IgG.

225 ysed using cell-based assays for MOG-IgG and aquaporin-4 immunoglobulin G (AQP4-IgG).

226 ltiple sclerosis, 8 primary CNS lymphoma, 84 aquaporin-4 immunoglobulin G positive, and 34 patients w

227 relapse risk versus placebo in patients with aquaporin-4 immunoglobulin G-positive neuromyelitis opti

228 uded 1047 patients, of whom 915 (87.4%) were aquaporin-4 immunoglobulin seropositive.

229 ment of patients with relapsed or refractory aquaporin 4-immunoglobulin G-seropositive neuromyelitis

230 All NMOSD patients were positive for aquaporin-4-immunoglobulin G, and all sarcoidosis cases

231 The tumor cells expressed aquaporin-4 immunoreactivity.

232 mmunopathologic studies suggest that loss of aquaporin-4 immunostaining is detectable in early lesion

233 markers, glial fibrillary acidic protein and aquaporin-4 immunostaining) at both time periods postisc

234 ein expression of the water channel protein, aquaporin 4 in these mice.

235 dicates that the autoimmune response against aquaporin-4 in neuromyelitis optica may be triggered by

236 ganization of the blood-brain barrier marker aquaporin-4 in the optic nerves were observed during the

237 otoxicity (ADCC) in cell cultures expressing aquaporin-4 in the presence of NMO autoantibody (NMO-IgG

238 hat the sarcolemmal localization of nNOS and aquaporin-4 in vivo depends on the presence of a dystrop

239 as no damage to maternal organs that express aquaporin-4, including the brain, spinal cord, kidneys,

240 tribution of endfoot proteins connexin43 and aquaporin-4, induces transcriptional changes in astrocyt

241 In the brain, the astrocytic water channel Aquaporin 4 is involved in clearance of amyloid beta, an

242 Aquaporin-4 is a mammalian water channel protein that is

243 Aquaporin-4 is abundant in brain and probably participat

244 In this study, we show that aquaporin-4 is expressed in the syncytiotrophoblast of h

245 al features of neuromyelitis optica and that aquaporin-4 is necessary and sufficient for immunoglobul

246 GPRC5B, like MLC1, GlialCAM and aquaporin-4, is expressed in astrocyte endfeet in human

247 tex in wild-type mice and 0.211 +/- 0.003 in Aquaporin-4 knockout mice.

248 ica are not solely dependent on IgG-mediated aquaporin-4 loss or lysis by complement or by IgG-depend

249 Focal astrocytopathy observed without aquaporin-4 loss or lytic complement component depositio

250 Aquaporin 4 may be a useful therapeutic target for strat

251 nt, non-NMO-IgG with human complement, or in aquaporin-4 null mice injected with NMO-IgG and human co

252 optica patients with human complement, or in aquaporin-4-null mice that received immunoglobulin G fro

253 enic autoantibodies target the water channel aquaporin-4 on human astrocytes causing neurological imp

254 totic, express glutamate receptors, and form aquaporin-4(+) perivascular endfeet.

255 localization of the astrocytic water channel aquaporin 4 persisted long after injury, recovering only

256 t of cerebral edema; 2) perivascular pool of aquaporin-4 plays a critical role in water egress from b

257 rospinal fluid was associated with increased aquaporin-4 polarization along astrocytic endfeet and di

258 (alpha-Syn(-/-)) that lack the perivascular aquaporin-4 pool but retain the endothelial pool of this

259 yn) that demonstrate diminished perivascular aquaporin-4 pool but retain the non-endfoot and ependyma

260 lux of water from brain via the perivascular aquaporin-4 pool.

261 od-brain barrier disruption via perivascular aquaporin-4 pool.

262 ian age of 39 years (range, 26-40 years) and aquaporin 4-positive NMO.

263 ferentiate NMOSD from MS, including all anti-aquaporin-4 protein (aAQP4)-antibody-negative patients w

264 Total aquaporin-4 protein expression was not different between

265 content, blood-brain barrier disruption, and aquaporin-4 protein expression were determined at 24 hou

266 Pregnancy-induced up-regulation of aquaporin-4 protein in brain and its role in eclampsia.

267 by a self-reactive Ab against the astrocyte aquaporin-4 protein.

268 vity between bacterial aquaporin-Z and human aquaporin-4 proteins.

269 euritis had extensive demyelination and lost aquaporin-4 reactivity.

270 Here, using Aquaporin 4 readthrough-specific knockout mice that stil

271 Labeling with the gliovascular marker aquaporin-4 revealed that at least half of the TH cells

272 ic and neuroimaging observations suggest the aquaporin-4-rich area postrema may be a first point of a

273 le compounds that enhance readthrough of the Aquaporin 4 sequence and validate a subset on endogenous

274 ould focus on areas of unmet need, including aquaporin-4 seronegative disease, and on development of

275 A patient with highly active aquaporin 4-seropositive NMO who failed numerous immunos

276 of NMO-IgG, and recent data suggesting that aquaporin-4-specific antibodies are pathogenic may enhan

277 M and associated proteins including Mlc1 and aquaporin-4 that is critical for control of GBM cell pro

278 s, an IgG autoantibody binding to astrocytic aquaporin 4, the principal water channel of the central

279 iated with the disease-specific autoantibody aquaporin-4, thought to be pathogenic.

280 arget antigens included CASPR2, LGI1, NMDAR, aquaporin 4, Tr (DNER [delta/notch-like epidermal growth

281 Less frequent were aquaporin-4, voltage-gated Kv1 potassium channel-complex

282 oss-immunoreactivity between aquaporin-Z and aquaporin-4 was investigated and ascertained in multiple

283 store sarcolemmal nNOS (although sarcolemmal aquaporin-4 was restored).

284 al fibrillary acidic protein (GFAP), or with aquaporin 4, was found in perivascular astrocytes of cor

285 abnormalities to be associated with loss of aquaporin-4 water and Kir4.1 potassium channels from gli

286 ting pathogenic autoantibodies targeting the aquaporin-4 water channel (AQP4).

287 patients have serum antibodies targeting the aquaporin-4 water channel expressed on the end-feet of a

288 Aquaporin-4 water channel gene deletion caused significa

289 Pathogenic antibodies targeting the aquaporin-4 water channel on astrocytes are associated w

290 e show that NMO-IgG binds selectively to the aquaporin-4 water channel, a component of the dystroglyc

291 s (neuromyelitis optica) a serum antibody to aquaporin-4 water channels has been detected.

292 n autoimmune inflammatory disorder targeting aquaporin-4 water channels in CNS astrocytes.

293 ific knockout mice that still express normal Aquaporin 4, we determine that this isoform indeed media

294 tive glia whereas GFAP and the water-channel aquaporin 4 were found at the periphery.

295 e, neuronal nitric oxide synthase (nNOS) and aquaporin-4 were absent from the sarcolemma.

296 etiformis and antibody test findings against aquaporin-4 were positive, leading to a diagnosis of neu

297 e gene encoding the astroglial water channel aquaporin-4, which is importantly involved in paravascul

298 This biomarker targets the water channel aquaporin-4, which is lost in neuromyelitis optica lesio

299 es comprised of three extracellular loops of aquaporin-4 with contributions from multiple molecules i

300 far have emphasized a characteristic loss of aquaporin-4, with deposition of IgG and complement and l